EGCG对羟自由基损伤小鼠胚胎海马神经元的保护作用

为了探讨表没食子儿茶素没食子酸酚(tea polyphenol(-)-epigallocatechin gal-late,EGCG)对羟自由基损伤小鼠海马神经元的保护作用,采用原代细胞培养技术,分离培养18 d小鼠胚胎海马神经元,培养4 d后,加入FeSO4和H2O2进行处理,随后加入不同浓度的EGCG培养24 h,通过观察细胞的形态学变化,四甲基偶氮唑盐(methylthiazolydi-phenyl-tetrazolium bromide,MTT)比色法分析细胞活性,检测神经元中丙二醛(malondi-aldehyde,MDA)以及培养液中乳酸脱氢酶(lactate dehydrogenase,LDH)含量的变化,以探讨EGCG对羟自由基损伤神经元的保护作用。结果显示,EGCG能够抑制神经元MDA的产生,降低神经元细胞外液中LDH的含量,增加细胞的活性,从而进一步证明EGCG能够清除羟自由基产生,减轻羟自由基对神经元损伤,对神经元的存活有一定的保护作用,为其用于治疗中枢神经系统病理性损伤的打下实验基础。

Effects of Tea Polyphenol (-)-Epigallocatechin Gallate Against Injury Induced by Hydroxyl Radical in Hippocampal Neuronsin vitro

To explore protective effects of tea polyphenol(-)-epigallocatechin gallate(EGCG) against injury induced by hydroxyl radical in cultured hippocampal neurons.primarily cultured neurons were dissociated from 18 day old embryonic mouse hippocampus,after being cultured 4 days in vitro.EGCG was added into medium to pretreat these cells at different concentrations following treatment of H_(2)O_(2).and FeSO_(4),then went on to cultured for 24 hours.Morphological changes of these cells were observed,neuronal viability was measured by MTT assay,in addition.malondialdehyde(MDA) of production in cultured neurons and levels of LDH in this media were detected.Eventually these changes were compared among different groups.This study indicated that EGCG can attenuate production of MDA in hippocamal neurons,decrease released levels of LDH in cultured media,and attenuate injury caused by hydroxyl radical,furthermore EGCG had neuroprotective effects on hippocampal neuronal survival.These results demonstated that EGCG may act further as neuroprotive agent against central nervous system pathological damage in clinical therapy.